To assess signalment, clinical findings, and treatments for New World camelids (NWCs) hospitalized for evaluation and treatment of neonatal disorders and investigate associations between these factors and death during and after hospitalization.
267 NWCs ≤ 30 days of age.
Medical records of a veterinary teaching hospital were retrospectively reviewed to identify NWCs admitted for evaluation and treatment of neonatal disorders between 2000 and 2010. Signalment, physical examination data, diagnostic findings, treatments, and outcomes were recorded. Factors were examined for association with death during hospitalization and the overall hazard of death by use of multivariable logistic regression and Cox proportional hazards analysis, respectively.
The sample comprised alpacas (n = 255) and llamas (12). Median age at admission was 3 days, and median hospitalization time was 2 days; 208 of the 267 (77.9%) neonatal NWCs survived to hospital discharge. Factors associated with increased odds of death during hospitalization included prematurity or dysmaturity, hypothermia, sepsis, toxic changes in neutrophils, and undergoing surgery. The odds of death during hospitalization also increased as anion gap increased. After discharge, 151 of 176 (85.8%) animals had follow-up information available (median follow-up time, 2,932 days); 126 (83%) were alive and 25 (17%) had died. Prematurity or dysmaturity, congenital defects, sepsis, oxygen administration, and undergoing surgery as a neonate were associated with an increased hazard of death; the hazard of death also increased as serum chloride concentration at the time of hospitalization increased.
CONCLUSIONS AND CLINICAL RELEVANCE
Results suggested the prognosis for survival during and after hospitalization is good for most NWCs hospitalized because of neonatal disorders.
Objective—To determine whether an inflammatory challenge induces insulin resistance in horses and examine possible contributions of adipose tissue to inflammatory cytokine production.
Animals—15 adult mares.
Procedures—Lipopolysaccharide (0.045 μg/kg, IV) or saline solution was administered, and insulin sensitivity was determined by means of the hyperinsulinemic, euglycemic clamp procedure or an adipose tissue biopsy was performed. Adipose tissue samples were collected, and mature adipocytes were obtained. Mature adipocytes were stimulated with lipopolysaccharide or dedifferentiated into preadipocytes and then stimulated with lipopolysaccharide. Interleukin-1, interleukin-6, and tumor necrosis factor A expression in blood, adipose tissue, and adipocytes was quantified with a real-time, reverse transcriptase– PCR assay.
Results—Lipopolysaccharide induced a transient increase in insulin sensitivity followed by a reduction in insulin sensitivity at 24 hours. Increased cytokine expression was observed in blood and adipose tissue following administration of lipopolysaccharide, and adipocytes and preadipocytes stimulated with lipopolysaccharide stained positive for tumor necrosis factor A. Expression of interleukin-1, interleukin-6, and tumor necrosis factor A was detected in preadipocytes stimulated with lipopolysaccharide, and interleukin-6 and tumor necrosis factor A were detected in mature adipocytes stimulated with lipopolysaccharide.
Conclusions and Clinical Relevance—Results indicated that insulin resistance develops following systemic inflammation in horses and suggested that adipose tissue may contribute to this inflammatory response. Methods to regulate insulin sensitivity may improve clinical outcome in critically ill patients.